Approximately 15 million people worldwide suffer a stroke each year, resulting in death or sensorimotor and other defects. Stroke remains the third most common cause of death in the industrialized world behind heart disease and cancer. There are two kinds of stroke: one is ischemic stroke, caused by a blood clot that blocks or prevents the flow of blood, and the other is hemorrhagic stroke, caused by bleeding into or around the brain.
Ischemic stroke is responsible for about one third of all deaths in industrialized countries and is the major cause of serious, long-term disability in adults over the age of 45. It stands to reason that there is a need for pharmacotherapy to treat acute ischemic stroke. Considerable insights have been gained into the mechanisms of stroke and the cascade of events that occurs following stroke; there is also an improved understanding of neuronal injury and cell death.
The three main mechanisms of ischemic stroke are thrombosis, embolism, and systemic hypoperfusion (with resultant ischemia and hypoxia). In each of these types of stroke, the area of the brain that dies as a result of the lack of blood supply thereto is called an infarct. Obstruction of a cerebral artery resulting from a thrombus that has built up on the wall of a brain artery is generally called “cerebral thrombosis.” In cerebral embolism, the occlusive material blocking the cerebral artery arises downstream in the circulation (e.g., an embolus is carried to the cerebral artery from the heart). Because it is difficult to discern whether a stroke is caused by thrombosis or embolism, the term “thromboembolism” is used to cover both these types of stroke. Systemic hypoperfusion may arise as a consequence of elevated blood lactate levels, reduced hematocrit, low blood pressure, or inability of the heart to pump blood adequately.
Also, the excessive or inappropriate stimulation of excitatory amino acid receptors leads to neuronal cell damage or loss by the way of a mechanism known as excitotoxicity. So, Excitatory amino acid excitotoxicity has been implicated in the pathophysiology of a number of neurological disorders. Such as stoke, cerebral ischemia and spinal cord trauma etc.
When symptoms of stroke last less than 24 hours and the patient recovers completely, the patient is said to have undergone a transient ischemic attack (TIA). The symptoms of TIA are a temporary impairment of speech, vision, sensation, or movement. Because a TIA is often thought to be a prelude to full-scale stroke, patients having suffered a TIA are candidates for prophylactic stroke therapy with anticoagulation agents (e.g., coumarin, and heparin) or anti-platelet agents (such as aspirin and ticlopidine), for example. But, in approximately 20% to 40% of patients with stroke, the underlying etiology is not established (called “cryptogenic,” “uncertain,” or “undetermined” stroke).
Therefore, a need exists for a therapy that is effective in the treatment all types of stroke, i.e., both ischemic strokes and hemorrhagic strokes.